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9 Cards in this Set
- Front
- Back
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2 major metabolites of THC
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OH-THC: active, plasma levels peak earlier
THC-COOH: inactive, plasma levels peak later ??levo isomer is more active?? |
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Absorption, Metabolism, Distribution, and Elimination
1. Psychotropic Threshold 2. Plasma levels 3. Metabolism 4. Distribution 5. Elimination |
1. psychotropic threshold >25 ng/ml
2. Drop to <2 ng/ml in 4 hours 3. Lipophilic: distributed into fatty tissues 4. cyt P450 5. 35% urine, 65% feces |
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Marijuana use detection
-Urine Test 1. Sensitivity 2. Window for use 3. Relation to plasma levels 4. Plasma Test |
1. Sensitive to 50 ng/ml, but cannot distinguish between THC or metabolites
2. single joint will test positive for 8-96 hours 3. Can have positive urine test for inactive metabolite long after active metabolite is gone. 4. Plasma samples correlate to time and amount used |
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Synthetic Cannabinoid Agonist
1. Name 2. 2 FDA approved uses |
1. Dronabinol
2. Nausea from chemotherapy and AIDS-related wasting |
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Cannabinoid receptor distribution
1. CB1 2. CB2 |
1. BRAIN, fat, liver, duodenum, muscle
2. LYMPHOCYTES > macrophages > cytokines |
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Endocannabinoids
1. Receptor preference 2. Name, abundance, and potency |
1. Bind CB1>CB2
2. -Annandamide: less abundant, more potent -2-Arachidonoyl glycerol: more abundant, less potent |
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CB1 receptors in the CNS
1. 6 dense areas 2. 3 moderate areas |
1. Dense: basal ganglia, cerebellum, hippocampus, NAcc, Middle prefrontal cortex, and parietal cortex
2. amygdala, spinal cord, and brainstem |
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Endocannabinoid Signalling
1. Name for the mechanism 2. Site of release 3. Site of action 4. Cellular response |
1. DISP: Depolarization-Induced Suppression of Inhibition
2. Postynaptic release upon stimulation 3. Presynaptic binding inhibits GABA and glutamate release (inhibitory nts.) 4. G Protein leads to decreased cAMP levels and other downstream effects |
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CB1 Anatagonists
1.Name 2/3.Potential therapeutic uses |
1. Rimonabant
2. Block direct reinforcing effects of drugs and food 3. Block motivational effects |
